Effects of norepinephrine on the electrical activities of pain-related neurons in the rat nucleus accumbens.

This study examined the effects of norepinephrine (NE) and phentolamine on the electrical activities of pain-excited neurons (PENs) and pain-inhibited neurons (PINs) in the nucleus accumbens (NAc) of Wistar rats. Trains of electric pulses applied to the right sciatic nerve were used to provide noxious stimulation, and the discharges of PENs and PINs were recorded using a glass microelectrode. Our results revealed that in response to noxious stimulation, NE decreases the evoked discharge frequency of PENs and increases the evoked discharge frequency of PINs in the NAc of healthy rats, whereas phentolamine produced opposite responses. These results demonstrate that NE is involved in the modulation of nociceptive information transmission in the NAc.

Noradrenergic mechanism involved in the nociceptive modulation of nociceptive-related neurons in the caudate putamen.

Norepinephrine (NE) participates in pain modulation of the central nervous system. The caudate putamen (CPu) is one region of the basal ganglia that has been demonstrated to be involved in nociceptive perception. Our previous work has shown that microinjection of different doses of norepinephrine into the CPu produces opposing effects in the tail-flick latency (TFL) of rats. However, the mechanism of action of NE on the pain-related neurons in the CPu remains unclear. The present study examined the effects of NE and the alpha-adrenoceptor antagonist phentolamine on the pain-evoked response of pain-excitation neurons (PENs) and pain-inhibition neurons (PINs) in the CPu of rats. Trains of electric impulses were used for noxious stimulation, and were applied to the sciatic nerve. The electrical activities of pain-related neurons in the CPu were recorded by a glass microelectrode. The results revealed that intra-CPu microinjection of NE (8microg/2microl) increased evoked firing frequency of PEN and shortened the firing latency, but decreased the evoked firing frequency of PIN and prolonged the inhibitory duration (ID). Intra-CPu administration of phentolamine (4microg/2microl) showed the opposite effects. The above results suggest that NE in the CPu modulates nociception by affecting the baseline firing rates of PENs and PINs.

MK-801 changes the role of glutamic acid on modulation of algesia in nucleus accumbens.

Dizocilpine maleate (MK-801) causes the blockage of the glutamic acid (Glu) receptors in the central nervous system that are involved in pain transmission. However, the mechanism of action of MK-801 in pain-related neurons is not clear, and it is still unknown whether Glu is involved in the modulation of this processing. This study examines the effect of MK-801, Glu on the pain-evoked response of pain-excitation neurons (PENs) and pain-inhibition neurons (PINs) in the nucleus accumbens (NAc) of rats. The trains of electric impulses applied to the sciatic nerve were used as noxious stimulation. The electrical activities of PENs or PINs in NAc were recorded by a glass microelectrode. Our results revealed that the lateral ventricle injection of Glu increased the discharged frequency and shortened the discharged latency of PEN, and decreased the discharged frequency and prolonged the discharged inhibitory duration (ID) of PIN in NAc of rats evoked by the noxious stimulation, while intra-NAc administration of MK-801 produced the opposite response. On the basis of above findings we can deduce that Glu, MK-801 and N-methyl-D-aspartate (NMDA) receptor are involved in the modulation of nociceptive information transmission in NAc.

Microinjection of different doses of norepinephrine into the caudate putamen produces opposing effects in rats.

It has been proven that norepinephrine (NE) regulates antinociception through its action on alpha-adrenoceptors located in brain nuclei, spinal cord, and peripheral organs. However, the supraspinal mechanism of noradrenergic pain modulation is controversial. The present study was aimed at investigating the nociceptive effects induced by injecting different doses of NE and phentolamine into the caudate putamen (CPU) of rats. The thermal pain threshold of the rats was measured by performing a tail-flick test. The tail-flick latency (TFL) was measured at 2-60 min after microinjection of the drugs. Our results revealed that the thermal pain threshold increased (long TFL) after the administration of a low dose of NE (2 microg/2 microl) and decreased (short TFL) after injection of a high dose of NE (8 microg/2 microl). In contrast, the pain threshold decreased after the administration of a low dose of phentolamine (1 microg/2 microl), while it increased after injection of a high dose of phentolamine (4 microg/2 microl). These results indicated that the injection of different doses of NE in the CPU of the rats produced opposite effects on the pain threshold, as determined by the tail-flick tests.

Cholecystokinin-8 antagonizes electroacupuncture analgesia through its B receptor in the caudate nucleus.

OBJECTIVES: The analgesic effect of electroacupuncture (EA) stimulation has been proved. However, its mechanism of action is not clear. It has been well-known that cholecystokinin-8 (CCK-8) is a neuropeptide which is mainly related to the mediation of pain. The caudate nucleus was selected to determine if the release of CCK and the neural activity in this nucleus were involved in producing EA analgesia. MATERIALS AND METHODS: Radiant heat focused on the rat-tail was used as the noxious stimulus. The pain threshold of rats was measured by tail-flick latency (TFL). EA stimulation at the bilateral Zusanli (ST 36) acupoints of rats was used to investigate the effects of EA analgesia. The electrical activities of pain-excited neurons (PEN) and pain-inhibited neurons (PIN) in the caudate nucleus were recorded with a glass microelectrode. The present study examined the antagonistic effects of the intracerebral ventricular injection of CCK-8 on EA analgesia and reversing effects of CCK-B receptor antagonist (L-365,260) injection into the caudate nucleus on CCK-8. RESULTS: The radiant heat focused on the tail of rats caused an increase in the evoked discharge of PEN and a reduction in the evoked discharge of PIN. EA stimulation at the bilateral ST 36 acupoints of rats resulted in the inhibition of PEN, the potentiation of PIN, and prolongation of TFL. The analgesic effect of EA was antagonized when CCK-8 was injected into the intracerebral ventricle of rats. The antagonistic effect of CCK-8 on EA analgesia was reversed by injection of CCK-B receptor antagonist (L-365,260) into the caudate nucleus of rats. CONCLUSIONS: Our results suggest that CCK-8 antagonize EA analgesia through its B receptor.

[Study on protective effect of vitamin E for ovarian grandlose cells and its mechanism in aged rats].

AIM: To observe the effect of vitamin E (VE) on ovarian apoptosis-related protein Bcl-2 and Bax and its impact on antioxidant capacity in aged female rats and to study the senility-delaying effect and mechanism of VE on ovary. METHODS: Natural aging female rats were given different doses of exogenous VE. Then apoptosis regulatory protein Bcl-2, Bax expression in ovarian grandlose cells were detected by using immunohistochemical methods and Western blot. The contents of serum total superoxide dismutase (SOD) activity and malondialdehyde (MDA) were detected by using biochemical methods. RESULTS: Contrasted with adult control group, the level of Bcl-2 expression in Senile control group was lower and the level of Bax expression was higher (P < 0.01), Serum SOD activity decreased and the level of MDA significantly increased (P < 0.01). Contrasted with senile control group, the level of Bcl-2 expression increased in VE group, the level of Bax expression decreased (P < 0.05), the level of MDA expression significantly decreased (P < 0.01). CONCLUSION: VE can regulate apoptosis-related protein Bcl-2, Bax expression and confront free radical damage which contribute to a protective effect for ovarian grandiose cells.